The objectives of this investigation are to a) further define the normal development of human cellular immunity, b) define abberations of development result from immaturity, neonatal illness, intrauterine malnutrition and postnatal malnutrition and c) investigate the mechanisms for the observed defects. Pediatric patients with increased susceptibility to infection will be studied, particularly high risk newborns with primary diseases, newborns small for gestational age as a result of intrauterine malnutrition and infants and children with acquired chronic malnutrition, including those undergoing hyperalimentation. Since past studies indicate that the cellular immune system is the most labile portion of the immune system, we postulate that deficiencies in the cellular immune system are responsible for the increased susceptibility to infection in these infants and children. Since the lymphocytes of newborns have well-established proliferative responses, we postulate that maturational defects will involve specialized functions such as mediator production and cytotoxicity, and monocyte function. Recent studies have shown that malnutrition and stress decreases the number and function of T lymphocytes. Additional studies in intrauterine and postnatal chronic malnutrition will further explore the nature and duration of these cellular immune defects. Cellular immune studies will include quantitating peripheral blood T and B lymphocytes and monocytes, measuring lymphocyte proliferative responses, assessing lymphocyte mediator production, assessing cytotoxicity of lymphocytes, and assessing monocyte function. In patients in which defects of the cellular immune system are noted, the mechanisms of such defects will be investigated by a) identifying the specific cell and function which is deficient, b) determining if suppressor cell activity is occurring, c) assessing specific nutrient levels, d) measuring plasma steroid hormones, e) assessing lymphocyte cyclic AMP and phosphodiesterase and f) investigating lymphocyte metabolic activity. The etiology of defects may thus be identified and correlated. BIBLIOGRAPHIC REFERENCE: Rich, K., Falk, P.M., Steihm, E.R., Feig., S., Golde, D.W., and Cline, M.J. Abnormal in vitro granulopoiesis in phenotypically normal parents of some children with congenital neutropenia. Pediatrics, 59: 396-400, 1977.